The mechanism(s) underlying the development of pulmonary edema are being investigated in rabbit lungs following oleic acid injury, volume overload, and re-expansion of chronically collapsed lung. Using 24Na and 131I-albumin as indicators of extravascular extracellular lung water and albumin, the rates of accumulation of water and albumin in lung interstitium have been characterized during the development of each type of pulmonary edema, and the concentration of albumin in interstitial water calculated. In normal control lungs, interstitial albumin concentration was 47% plus or minus S.E. 3.8 of the plasma albumin concentration (lung/plasma albumin concentration). Following oleic acid injection, the lung/plasma albumin concentration rose to 105% plus or minus S.E. 14 at three hours. Volume overload with plasma resulted in no change in lung/plasma albumin concentration with infusions of 70 ml/kg over one hour. When the volume of infusion was increased to approximately 150 ml/kg over two hours, the lung/plasma albumin concentration increased to 84%. Rapid re-expansion of chronically collapsed lung also resulted in increased lung water and lung/plasma albumin concentration. The results suggest that vascular injury with increased permeability to blood proteins may be a common mechanism underlying the development of acute pulmonary edema due to fat embolism, acute increases of hydrostatic pressure (acute congestive heart failure), and re-expansion of chronically collapsed lung.